Evidence map›Paper›PMID 38610044›Full record

ArticleEuropean journal of medical research2024

Tyrosine hydroxylase inhibits HCC progression by downregulating TGFβ/Smad signaling.

Guoqian Liu, Mengwei Li, Zimei Zeng, Qi Fan, Xinxin Ren, Zhexin Wang, Yaoqi Sun, Yulin He, Lunquan Sun, Yuezhen Deng and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 91% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 0 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Guoqian Liu *Key Laboratory of Molecular Radiation Oncology Hunan Province, Changsha, 410008, Hunan, China.
Mengwei Li *Key Laboratory of Molecular Radiation Oncology Hunan Province, Changsha, 410008, Hunan, China.
Zimei ZengDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Qi FanDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Xinxin RenCancer Center, Department of Pathology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, 310014, Zhejiang, China.
Zhexin WangDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yaoqi SunDepartment of Obstetrics and Gynecology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yulin HeDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Lunquan SunKey Laboratory of Molecular Radiation Oncology Hunan Province, Changsha, 410008, Hunan, China.
Yuezhen DengDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. 7280002719@shsmu.edu.cn.
Shupeng LiuDepartment of Obstetrics and Gynecology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. lshup@tongji.edu.cn.
Chenxi ZhongDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. schleomon@163.com.
Jie GaoKey Laboratory of Molecular Radiation Oncology Hunan Province, Changsha, 410008, Hunan, China. 15575974972@163.com.
Shanghai Jiao Tong University · CNShanghai Chest Hospital · CNHangzhou Medical College · CNShanghai Tenth People's Hospital · CNTongji University · CN

Funding

Hunan Provincial Science and Technology Department 2021JJ30039National Natural Science Foundation of China 82172980
6 · The paper itself

Abstract

The alteration of metabolic processes has been found to have significant impacts on the development of hepatocellular carcinoma (HCC). Nevertheless, the effects of dysfunction of tyrosine metabolism on the development of HCC remains to be discovered. This research demonstrated that tyrosine hydroxylase (TH), which responsible for the initial and limiting step in the bio-generation of the neuro-transmitters dopamine and adrenaline, et al. was shown to be reduced in HCC. Increased expression of TH was found facilitates the survival of HCC patients. In addition, decreased TH indicated larger tumor size, much more numbers of tumor, higher level of AFP, and the presence of cirrhosis. TH effectively impairs the growth and metastasis of HCC cells, a process dependent on the phosphorylation of serine residues (S19/S40). TH directly binds to Smad2 and hinders the cascade activation of TGFβ/Smad signaling with the treatment of TGFβ1. In summary, our study uncovered the non-metabolic functions of TH in the development of HCC and proposes that TH might be a promising biomarker for diagnosis as well as an innovative target for metastatic HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell LineHumansSignal TransductionTyrosine 3-MonooxygenaseTyrosine 3-MonooxygenaseCancer metabolismHepatocellular carcinomaTGFβ/Smad signalingTyrosine hydroxylase

Identifiers

PMID38610044
PMCPMC11015545
OpenAlexW4394749805

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.